PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29463871-10	2018	Conversely, withdrawal of the combination clonidine/GRK2-inhibitor treatment did not cause rebound hypertension, and normal induction of endothelium-dependent relaxation, decreased GRK2 activity, and increased Akt/eNOS were observed in aortas from DM mice.	Clonidine	42-51	G protein-coupled receptor kinase 2	Mus musculus	181-185	
29463871-9	2018	At 21 days, clonidine withdrawal triggered rebound hypertension together with impaired endothelium-dependent relaxation, increased GRK2 activity, and reduced Akt/endothelial NO synthase (eNOS)/NO production in aortas.	Clonidine	12-21	G protein-coupled receptor kinase 2	Mus musculus	131-135	
29463871-0	2018	Co-treatment with clonidine and a GRK2 inhibitor prevented rebound hypertension and endothelial dysfunction after withdrawal in diabetes.	Clonidine	18-27	G protein-coupled receptor kinase 2	Mus musculus	34-38	
22925038-12	2013	CONCLUSION: GRK2 plays a key role in modulating the aortic vasodilator effect of clonidine by selectively affecting the Akt/eNOS pathway.	Clonidine	81-90	G protein-coupled receptor kinase 2	Mus musculus	12-16	
22581458-5	2012	The GRK2 inhibitor significantly improved clonidine-induced relaxation only in diabetic (ob/ob and DM) mice, with accompanying attenuations of GRK2 activity and translocation to the plasma membrane.	Clonidine	42-51	G protein-coupled receptor kinase 2	Mus musculus	4-8	
22581458-6	2012	These protective effects of the GRK2 inhibitor may be attributable to the augmented Akt/eNOS pathway activation (as evidenced by increases in Akt phosphorylation at Ser(473) and at Thr(308), and eNOS phosphorylation at Ser(1177)) and to the prevention of the GRK2 translocation and promotion of beta-arrestin 2 translocation to the membrane under clonidine stimulation.	Clonidine	347-356	G protein-coupled receptor kinase 2	Mus musculus	32-36	
22581458-8	2012	Our work provides the first evidence that in diabetes, the GRK2 inhibitor ameliorates vascular endothelial dysfunction via the Akt/eNOS pathway by inhibiting GRK2 activity and enhancing beta-arrestin 2 translocation under clonidine stimulation, thereby contributing to a blood pressure-lowering effect.	Clonidine	222-231	G protein-coupled receptor kinase 2	Mus musculus	59-63	
21571071-9	2011	In the diabetics, the clonidine-induced responses (but not the insulin-induced ones) were enhanced by GRK2-inhibitor.	Clonidine	22-31	G protein-coupled receptor kinase 2	Mus musculus	102-106	
21571071-11	2011	The phosphorylation of Akt at Thr308 was significantly normalized and the phosphorylation of eNOS at Ser1177 tended to be increased by GRK2-inhibitor in the clonidine-stimulated diabetics.	Clonidine	157-166	G protein-coupled receptor kinase 2	Mus musculus	135-139